Figure 5.
The IRF5 inhibitor MS19 inhibits IL-6 production from cGVHD B cells. (A) B cells isolated from healthy donors were stimulated with 1 μg/mL TLR7 agonist R848, the TLR9 agonist CpG, or the TLR4 agonist LPS for 24 hours after incubation with the AAAG-rich microsatellite inhibitor MS19 (5 μg/mL; blue triangles) or control media (red circles) to inhibit IRF5 nuclear translocation. Production of IL-6 in B-cell supernatants was measured via ELISA and compared between MS19 and control media groups (n = 9 per group). (B) B cells isolated from patients with active cGVHD were incubated with varying doses of MS19 and then stimulated with R848 or CpG for 24 hours or left unstimulated. B-cell supernatants were harvested and examined for IL-6 production by ELISA. Within individual stimulation conditions, statistics were performed between the MS19 groups at all doses and the no-MS19 group (n = 4 per group). ∗P < .05 and ∗∗P < .01 between sample groups. Data represent median ± range.

The IRF5 inhibitor MS19 inhibits IL-6 production from cGVHD B cells. (A) B cells isolated from healthy donors were stimulated with 1 μg/mL TLR7 agonist R848, the TLR9 agonist CpG, or the TLR4 agonist LPS for 24 hours after incubation with the AAAG-rich microsatellite inhibitor MS19 (5 μg/mL; blue triangles) or control media (red circles) to inhibit IRF5 nuclear translocation. Production of IL-6 in B-cell supernatants was measured via ELISA and compared between MS19 and control media groups (n = 9 per group). (B) B cells isolated from patients with active cGVHD were incubated with varying doses of MS19 and then stimulated with R848 or CpG for 24 hours or left unstimulated. B-cell supernatants were harvested and examined for IL-6 production by ELISA. Within individual stimulation conditions, statistics were performed between the MS19 groups at all doses and the no-MS19 group (n = 4 per group). ∗P < .05 and ∗∗P < .01 between sample groups. Data represent median ± range.

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